Purpose:

Rheumatoid arthritis (RA) is a multi-organ inflammatory disorder associated with high cardiovascular morbidity and mortality. Using contrast enhanced cardiac magnetic resonance imaging (cMR) with pharmacologic stress, we sought to identify microvascular impairment and myocardial inflammation/fibrosis in a group of RA patients and explore the association of these outcomes with RA disease characteristics.

Methods:

RA patients with no history and/or clinical findings of systemic hypertension, coronary artery disease, severe valvular heart disease, atrial fibrillation, diabetes mellitus, or echocardiographic abnormalities underwent contrast-enhanced cMR on a 1.5T scanner. Adenosine triphosphate was used to assess perfusion defects due to microvascular impairment or ischemia, and delayed enhanced imaging was obtained for the assessment of myocardial inflammation/fibrosis. We evaluated the associations of cMR abnormalities with RA disease activity and severity measures.

Result:

Eighteen patients (72% female) with a mean age of 57 ± 10 years were studied. The mean DAS28 for the cohort was 3.96, with 6 participants (33.3%) falling into the low disease activity category (DAS28<3.2) and 6 participants (33.3%) falling into the high disease activity category (DAS28>5.1). Eight patients (45%) demonstrated a myocardial abnormality. Stress perfusion defects were seen in two patients (11%), one of whom had a circumferential subendocardial perfusion defect and one had a non-segmental subendocardial perfusion defect. Seven patients (39%) were found to have delayed enhancement (indicating myocardial inflammation or fibrosis), only one of whom also demonstrated a perfusion defect. Mean DAS28 was significantly higher in the group with delayed enhancement compared to the group without by an average of 1.32 DAS28 units (4.77 vs. 3.44 units, respectively; p=0.011). Corresponding trends to statistical significance were noted in systemic inflammatory markers, with both CRP and ESR quantitatively higher in the group with delayed enhancement. Despite higher disease activity overall, TNF inhibitors were prescribed in only one participant with delayed enhancement (14.3%) compared to 6 without delayed enhancement (54.6%); however, this difference was not statistically significant (p=0.15). Other RA characteristics were not significantly associated with myocardial abnormalities.

Conclusion:

Myocardial involvement, as detected by cMR, was frequent in RA patients without known cardiac disease. Myocardial inflammation/fibrosis was observed more frequently than microvascular impairment and, combined with its association with higher RA disease activity, suggests a mechanistic connection between articular and myocardial inflammation in RA.